Exercise is a potent stimulus against cardiac ischemia reperfusion (IR) injury, although the protective mechanisms are not completely understood. The study purpose was to examine whether the mitochondrial or sarcolemmal ATP-sensitive potassium channel (mito K(ATP) or sarc K(ATP), respectively) mediates exercise-induced cardioprotection against post-IR cell death and apoptosis. Eighty-six, 4-mo-old male Sprague Dawley rats were randomly assigned to treadmill exercise (Ex; 30 m/min, 3 days, 60 min, ∼70 maximal oxygen uptake) and sedentary (Sed) treatments. Rats were exposed to regional cardiac ischemia (50 min) and reperfusion (120 min) or Sham (170 min; no ligation) surgeries. Exercise subgroups received placebo (saline), 5-hydroxydecanoate (5HD; 10 mg/kg ip), or HMR1098 (10 mg/kg ip) to inhibit mito K(ATP) or sarc K(ATP) channel. Comprehensive outcome assessments included post-IR ECG arrhythmias, cardiac tissue necrosis, redox perturbations, and autophagy biomarkers. No arrhythmia differences existed between exercised and sedentary hearts following extended-duration IR (P < 0.05). The sarc K(ATP) channel was confirmed essential (P = 0.002) for prevention of antinecrotic tissue death with exercise (percent infarct, Sed = 42%; Ex = 20%; Ex5HD = 16%; ExHMR = 42%), although neither the mito K(ATP) (P = 0.177) nor sarc K(ATP) (P = 0.274) channel provided post-IR protection against apoptosis (terminal deoxynucleotidyl transferase deoxy UTP-mediated nick-end labeling-positive nuclei/mm(2), Sham = 1.8 ± 0.5; Sed = 19.4 ± 6.7; Ex = 7.5 ± 4.6; Ex5HD = 14.0 ± 3.9; ExHMR = 11.1 ± 1.8). Exercise preconditioning also appears to preserve basal autophagy levels, as assessed by Beclin 1 (P ≤ 0.001), microtubule-associated protein-1 light-chain 3B ratios (P = 0.020), and P62 (P ≤ 0.001), in the hours immediately following IR. Further research is needed to better understand these findings and corresponding redox changes in exercised hearts.

In this study, we examined the relationship between serum creatine kinase activity following exercise-induced muscle damage and muscle fibre composition. Seventeen untrained males volunteered and underwent a .[Vdot]O2max test, Wingate test, and an exercise-induced muscle damage protocol. Muscle soreness and blood samples were recorded before, immediately after, and 24, 48, 72, and 96 h after exercise. Biopsy samples from the vastus lateralis were collected one week after exercise-induced muscle damage and were assessed for muscle fibre composition. There was no significant relationship (P > 0.05) between muscle fibre composition and creatine kinase activity. A significant positive correlation (P < 0.05) was observed between soreness 48 h after exercise and type II and IIb fibres, and a significant negative correlation (P < 0.05) was observed between soreness 48 h after exercise and type I muscle fibres. Significant positive correlations were observed between soreness 48 h after exercise and the fatigue index, relative average power, and relative anaerobic capacity. Our results suggest that creatine kinase activity following exercise-induced muscle damage may not be related to muscle fibre proportions, and higher post-exercise muscular pain may be related to a predominance of type II muscle fibres and higher anaerobic capabilities.

The purpose of this study was to compare mechanical efficiency between repeated static jumps (SJ), countermovement jumps (CMJ), drop jumps from 75% of maximum CMJ jump height (75DJ) and drop jumps from 125% of maximum CMJ height (125DJ). Subjects included eight jump-trained males. All subjects completed 30 continuous repetitions in the SJ, CMJ, 75DJ, and 125DJ. Oxygen consumption, peak force and center of mass displacement for each repetition during the four jumping patterns were measured. ME was calculated from a combination of force-time curves, displacement-time curves and lactate-corrected oxygen consumption values. In addition, muscle activity was recorded from the vastus medialis, vastus lateralis and biceps femoris using surface electromyography (EMG). 125DJ and 75DJ resulted in significantly (P < or = 0.05) greater ME in comparison to CMJ and SJ. CMJ resulted in significantly greater ME in comparison to SJ. In addition, braking phase muscle activity was significantly greater in 125DJ and 75DJ in comparison to CMJ. Negative work was significantly different between 125DJ, 75DJ and CMJ (125DJ > 75DJ > CMJ). There was a significant positive correlation (r = 0.68) between ME and negative work performed across 125DJ, 75DJ and CMJ. These findings suggest that stretch-shortening cycle movements, which include a strenuous braking phase combined with simultaneous high muscle activity, increase ME. This may be due to optimal muscle-tendon unit kinetics and usage of stored elastic energy.

Acute strength exercise elicits a transient oxidative stress, but the factors underlying the magnitude of this response remain unknown. The purpose of this investigation was to determine whether muscle-fiber type relates to the magnitude of blood oxidative stress after eccentric muscle activity. Eleven college-age men performed 3 sets of 50 eccentric knee-extensions. Blood samples taken pre-, post-, and 24, 48, 72, and 96 hr postexercise were assayed for comparison of muscle damage and oxidative-stress biomarkers including protein carbonyls (PCs). Vastus lateralis muscle biopsies were assayed for relative percentage of slow- and fast-twitch muscle fibers. There was a mixed fiber composition (Type I = 39.6% ± 4.5%, Type IIa = 35.7% ± 3.5%, Type IIx = 24.8% ± 3.8%; p = .366). PCs were elevated 24, 48, and 72 hr (p = .032) postexercise, with a peak response of 126% (p = .012) above baseline, whereas other oxidative-stress biomarkers were unchanged. There are correlations between Type II muscle-fiber type and postexercise PC. Further study is needed to understand the mechanisms responsible for the observed fast-twitch muscle-fiber oxidative-stress relationship.

No abstract